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Exosomes derived from cardiac microvascular endothelial cells (CMECs) under hypoxia can mediate cardiac repair functions and alleviate pyroptosis and oxidative stress during ischemia\u2010reperfusion (I\/R) injury. This study is aimed at investigating the effect and mechanism of miR\u201027b\u20103p underlying hypoxic CMECs\u2010derived exosomes against I\/R injury. <jats:italic>Methods<\/jats:italic>. CMECs were isolated from the left ventricle of Sprague\u2010Dawley rats, followed by culturing under hypoxic conditions or pretreatment with the miR\u201027b\u20103p inhibitor. CMECs\u2010derived exosomes were added into H9C2 cells before hypoxia\/reoxygenation (H\/R) or injected into the rat heart before I\/R injury. An <jats:italic>in vivo<\/jats:italic> I\/R injury model was established by ligating and releasing the left anterior descending coronary artery. Expression of pyroptosis\u2010related factors was detected using Western blot, and heart infarcted size was determined by the 2,3,5\u2010triphenyl\u20102H\u2010tetrazpinolium chloride staining method. Dual\u2010Luciferase Reporter assays were performed to analyze the interactions of nmiR\u201027b\u20103p\u2010forkhead box O1 (Foxo1) and Gasdermin D\u2010 (GSDMD\u2010) Foxo1. Chromatin\u2010immunoprecipitation (ChIP) assays were performed to validate the interactions between forkhead box O1 (Foxo1) and Gasdermin D (GSDMD) and Foxo1\u2010mediated histone acetylation of GSDMD. <jats:italic>Results<\/jats:italic>. CMECs were successfully identified from left ventricle of Sprague\u2010Dawley rats. The expressions of Foxo1 and pyroptosis\u2010related proteins (GSDMD, NLPR3, cleaved caspase 1, IL\u20101<jats:italic>\u03b2,<\/jats:italic> and IL\u201018) were upregulated in the rat heart after I\/R injury. Treatment of CMEC\u2010derived exosomes, especially that under hypoxic conditions, significantly reduced pyroptosis in the rat heart. miR\u201027b\u20103p was significantly upregulated in CMEC\u2010derived exosomes under hypoxic conditions, and miR\u201027b\u20103p inhibition in exosomes alleviated its cytoprotection and inhibited oxidative stress in H9C2 cells. Treatment with Foxo1 overexpression plasmids aggravated <jats:italic>in vitro<\/jats:italic> H\/R and <jats:italic>in vivo<\/jats:italic> I\/R injury by upregulating pyroptosis\u2010related proteins. Further experiments validated that miR\u201027b\u20103p negatively targeted Foxo1, which bound to the promoter region of GSDMD. <jats:italic>Conclusions<\/jats:italic>. These results demonstrated a great therapeutic efficacy of miR\u201027b\u20103p overexpression in hypoxic CMEC\u2010derived exosomes in preventing the development of myocardial damage post I\/R injury through inhibiting Foxo1\/GSDMD signaling\u2010induced oxidative stress and pyroptosis.<\/jats:p>","DOI":"10.1155\/2022\/8215842","type":"journal-article","created":{"date-parts":[[2022,7,6]],"date-time":"2022-07-06T21:35:22Z","timestamp":1657143322000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["[Retracted] Exosomal miR\u201027b\u20103p Derived from Hypoxic Cardiac Microvascular Endothelial Cells Alleviates Rat Myocardial Ischemia\/Reperfusion Injury through Inhibiting Oxidative Stress\u2010Induced Pyroptosis via Foxo1\/GSDMD 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